Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Thursday, August 15, 2013

Is Tumor Necrosis Factor-α Friend or Foe for Chronic Heart Failure?

What researcher or stroke association is going to answer the same question about stroke?
http://circres.ahajournals.org/content/113/5/492.extract.html?etoc
Although detrimental effects of tumor necrosis factor-α (TNF-α) have been reported in failing myocardium, clinical trials using TNF-α antagonists did not show the benefit of TNF-α inhibition in patients with chronic heart failure (CHF). The double-edged effects of TNF-α/Toll-like receptors (TLRs)–related proinflammatory cytokines and downstream signal transduction, nuclear factor (NF)-κB activation on failing myocardium are discussed.
It is well known that neurohormonal activation in heart failure plays a key role in deterioration of myocardial failure, accelerating the vicious cycle in pathophysiology of heart failure. Proinflammatory cytokines are also increased in patients with heart failure. Since the first report by Levine et al1 that serum TNF-α is increased in patients with severe heart failure, other cytokines, such as interleukin-1β (IL-1β), interleukin-6 (IL-6), and their soluble receptors, have been reported to increase in heart failure.2 Several reports indicated that plasma levels of these proinflammatory cytokines are correlated with severity of heart failure, New York Heart Association functional class.3 The question was whether these proinflammatory cytokines deteriorate the failing myocardium as a cause of detrimental mechanism or merely secondary phenomenon in heart failure.
To answer this question, Kubota et al4 established a murine transgenic line of TNF-α in which expression was driven by the murine α-myosin heavy chain promoter. The transgenic heart with chronic overexpression of TNF-α showed (1) ventricular hypertrophy, (2) ventricular dilatation, (3) interstitial infiltrates, (4) interstitial fibrosis, (5) rare myocyte apoptosis, (6) a diminished ejection fraction, (7) attenuation of β1-adrenergic responsiveness, and (8) expression of atrial …

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